Mol. Hum. Reprod. Advance Access originally published online on January 10, 2006
Molecular Human Reproduction 2005 11(11):801-808; doi:10.1093/molehr/gah240
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Progesterone-dependent release of transforming growth factor-beta1 from epithelial cells enhances the endometrial decidualization by turning on the Smad signalling in stromal cells
1Department of Obstetrics and Gynecology, Ajou University School of Medicine and 2Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea
3 To whom correspondence should be addressed at: Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea. E-mail: minc{at}ajou.ac.kr
Endometrial decidualization results from the differentiation of stromal cells in an ovarian steroid-sensitive manner. Human endometrial tissues obtained from fertile women at various stages of the menstrual cycle were subjected to immunohistochemistry to localize the components of the transforming growth factor-beta (TGF-ß) system. TGF-ß receptor-I and -II expression was higher in stromal cells than in epithelial cells during the secretory phase while no such variation was observed during the proliferative phase. The expression of phosphorylated Smad3 (pSmad2/3), an activated form of a component of the TGF-ß signalling pathway, and translocation of pSmad2/3 from the cytoplasm to the nucleus were more pronounced in secretory endometrium. In coculture of human endometrial epithelial with stromal cells, each isolated from the proliferative endometrium, administration of progesterone stimulated decidualization as well as TGF-ß signalling activation in stromal cells. Progesterone also significantly elevated the concentration of TGF-ß1 in the coculture medium. Careful manipulation of the coculture, i.e. selective addition and omission of the cellular components, showed that this progesterone-induced increase in secretion of TGF-ß1 come mainly from epithelial cells. Moreover, administration of TGF-ß1 (10 ng/ml) directly to cultured stromal cells enhanced the expression of prolactin as well as pSamd2/3 even without progesterone. Taken together, our present data support the notion that progesterone induces stromal decidualization indirectly, i.e. by enhancing the expression and secretion of TGF-ß1 from epithelial cells. The secreted, epithelial-derived TGF-ß1 then acts on adjacent stromal cells, at least in part, to turn on Smad signalling that could lead to stromal decidualization.
Key words: coculture of human endometrial epithelial and stromal cells/endometrial decidualization/paracrine mediator/Smad signalling/TGF-ß1
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